Series: Volume 3, Issue 1 2012

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The ethics of euthanasia

Introduction

The topic of euthanasia is one that is shrouded with much ethical debate and ambiguity. Various types of euthanasia are recognised, with active voluntary euthanasia, assisted suicide and physicianassisted suicide eliciting the most controversy. [1] Broadly speaking, these terms are used to describe the termination of a person’s life to end their suffering, usually through the administration of drugs. Euthanasia is currently illegal in all Australian states, refl ecting the status quo of most countries, although, there are a handful of countries and states where acts of euthanasia are legally permitted under certain conditions.

Advocates of euthanasia argue that people have a right to make their own decisions regarding death, and that euthanasia is intended to alleviate pain and suffering, hence being ascribed the term “mercy killing.” They hold the view that active euthanasia is not morally worse than the withdrawal or withholding of medical treatment, and erroneously describe this practice as “passive euthanasia.” Such views are contested by opponents of euthanasia who raise the argument of the sanctity of human life and that euthanasia is equal to murder, and moreover, abuses autonomy and human rights. Furthermore, it is said that good palliative care can provide relief from suffering to patients and unlike euthanasia, should be the answer in modern medicine. This article will define several terms relating to euthanasia in order to frame the key arguments used by proponents and opponents of euthanasia. It will also outline the legal situation of euthanasia in Australia and countries abroad.

Defining euthanasia

The term “euthanasia” is derived from Greek, literally meaning “good death”. [1] Taken in its common usage however, euthanasia refers to the termination of a person’s life, to end their suffering, usually from an incurable or terminal condition. [1] It is for this reason that euthanasia was also coined the name “mercy killing”.

Various types of euthanasia are recognised. Active euthanasia refers to the deliberate act, usually through the intentional administration of lethal drugs, to end an incurably or terminally ill patient’s life. [2] On the other hand, supporters of euthanasia use another term, “passive euthanasia” to describe the deliberate withholding or withdrawal of life-prolonging medical treatment resulting in the patient’s death. [2] Unsurprisingly, the term “passive euthanasia” has been described as a misnomer. In Australia and most countries around the world, this practice is not considered as euthanasia at all. Indeed, according to Bartels and Otlowski [2] withholding or withdrawing life-prolonging treatment, either at the request of the patient or when it is considered to be in the best interests of the patient, “has become an established part of medical practice and is relatively uncontroversial.”

Acts of euthanasia are further categorised as “voluntary”, “involuntary” and “non-voluntary.” Voluntary euthanasia refers to euthanasia performed at the request of the patient. [1] Involuntary euthanasia is the term used to describe the situation where euthanasia is performed when the patient does not request it, with the intent of relieving their suffering – which, in effect, amounts to murder. [3] Non-voluntary euthanasia relates to a situation where euthanasia is performed when the patient is incapable of consenting. [1] The term that is relevant to the euthanasia debate is “active voluntary euthanasia”, which collectively refers to the deliberate act to end an incurable or terminally ill patient’s life, usually through the administration of lethal drugs at his or her request. The main difference between active voluntary euthanasia and assisted suicide is that in assisted suicide and physician-assisted suicide, the patient performs the killing act. [2] Assisted suicide is when a person intentionally assists a patient, at their request, to terminate his or her life. [2] Physician-assisted suicide refers to a situation where a physician intentionally assists a patient, at their request, to end his or her life, for example, by the provision of information and drugs. [3]

Another concept that is linked to end-of-life decisions and should be differentiated from euthanasia is the doctrine of double effect. The doctrine of double effect excuses the death of the patient that may result, as a secondary effect, from an action taken with the primary intention of alleviating pain. [4] Supporters of euthanasia may describe this as indirect euthanasia, but again, this term should be discarded when considering the euthanasia debate. [3]

Legal situation of active voluntary euthanasia and assisted suicide

In Australia, active voluntary euthanasia, assisted suicide and physician-assisted suicide are illegal (see Table 1). [1] In general, across all Australian states and territories, any deliberate act resulting in the death of another person is defined as murder. [2] The prohibition of euthanasia and assisted suicide is established in the criminal legislation of each Australian state, as well as the common law in the common law states of New South Wales, South Australia and Victoria. [2]

The prohibition of euthanasia and assisted suicide in Australia has been the status quo for many years now. However, there was a period when the Northern Territory permitted euthanasia and physician-assisted suicide under the Rights of Terminally Ill Act (1995). The Act came into effect in 1996 and made the Northern Territory the first place in the world to legally permit active voluntary euthanasia and physicianassisted suicide. Under this Act, competent terminally ill adults who were aged 18 or over, were able to request a physician to help them in dying. This Act was short-lived however, after the Federal Government overturned it in 1997 with the Euthanasia Laws Act 1997. [1,2] The Euthanasia Laws Act 1997 denied states the power to legislate to permit euthanasia or assisted suicide. [1] There have been a number of attempts in various Australian states, over the past decade and more recently, to legislate for euthanasia and assisted suicide, but all have failed to date, owing to a majority consensus against euthanasia. [1]

A number of countries and states around the world have permitted euthanasia and/or assisted suicide in some form; however this is often under specific conditions (see Table 2).

Arguments for and against euthanasia

There are many arguments that have been put forward for and against euthanasia. A few of the main arguments for and against euthanasia are outlined below.

For

Rights-based argument

Advocates of euthanasia argue that a patient has the right to make the decision about when and how they should die, based on the principles of autonomy and self-determination. [1, 5] Autonomy is the concept that a patient has the right to make decisions relating to their life so long as it causes no harm to others. [4] They relate the notion of autonomy to the right of an individual to control their own body, and should have the right to make their own decisions concerning how and when they will die. Furthermore, it is argued that as part of our human rights, there is a right to make our own decisions and a right to a dignified death. [1]

Beneficence

It is said that relieving a patient from their pain and suffering by performing euthanasia will do more good than harm. [4] Advocates of euthanasia express the view that the fundamental moral values of society, compassion and mercy, require that no patient be allowed to suffer unbearably, and mercy killing should be permissible. [4]

The difference between active euthanasia and passive euthanasia

Supporters of euthanasia claim that active euthanasia is not morally worse than passive euthanasia – the withdrawal or withholding of medical treatments that result in a patient’s death. In line with this view, it is argued that active euthanasia should be permitted just as passive euthanasia is allowed.

James Rachels [12] is a well-known proponent of euthanasia who advocates this view. He states that there is no moral difference between killing and letting die, as the intention is usually similar based on a utilitarian argument. He illustrates this argument by making use of two hypothetical scenarios. In the first scenario, Smith anticipates an inheritance should anything happen to his six-year-old cousin, and ventures to drown the child while he takes his bath. In a similar scenario, Jones stands to inherit a fortune should anything happen to his six-year-old cousin, and upon intending to drown his cousin, he witnesses his cousin drown on his own by accident and lets him die. Callahan [9] highlights the fact that Rachels uses a hypothetical case where both parties are morally culpable, which fails to support Rachels’ argument.

Another of his arguments is that active euthanasia is more humane than passive euthanasia as it is “a quick and painless” lethal injection whereas the latter can result in “a relatively slow and painful death.” [12]

Opponents of euthanasia argue that there is a clear moral distinction between actively terminating a patient’s life and withdrawing or withholding treatment which ends a patient’s life. Letting a patient die from an incurable disease may be seen as allowing the disease to be the natural cause of death without moral culpability. [5] Life-support treatment merely postpones death and when interventions are withdrawn, the patient’s death is caused by the underlying disease. [5]

Indeed, it is this view that is strongly endorsed by the Australian Medical Association, who are opposed to voluntary active euthanasia and physician-assisted suicide, but does not consider the withdrawal or withholding of treatment that result in a patient’s death as euthanasia or physician-assisted suicide. [1]

Against

The sanctity of life

Central to the argument against euthanasia is society’s view of the sanctity of life, and this can have both a secular and a religious basis. [2] The underlying ethos is that human life must be respected and preserved. [1]

The Christian view sees life as a gif offerrom God, who ought not to be off ended by the taking of that life. [1] Similarly the Islamic faith says that “it is the sole prerogative of God to bestow life and to cause death.” [7] The withholding or withdrawal of treatment is permitted when it is futile, as this is seen as allowing the natural course of death. [7]

Euthanasia as murder

Society views an action which has a primary intention of killing another person as inherently wrong, in spite of the patient’s consent. [8] Callahan [9] describes the practice of active voluntary euthanasia as “consenting adult killing.”

Abuse of autonomy and human rights

While autonomy is used by advocates for euthanasia, it also features in the argument against euthanasia. Kant and Mill [3] believe that the principle of autonomy forbids the voluntary ending of the conditions necessary for autonomy, which would occur by ending one’s life.

It has also been argued that patients’ requests for euthanasia are rarely autonomous, as most terminally ill patients may not be of a sound or rational mind. [10]

Callahan [9] argues that the notion of self-determination requires that the right to lead our own lives is conditioned by the good of the community, and therefore we must consider risk of harm to the common good.

In relation to human rights, some critics of euthanasia argue that the act of euthanasia contravenes the “right to life”. The Universal Declaration of Human Rights highlights the importance that, “Everyone has the right to life.” [3] Right to life advocates dismiss claims there is a right to die, which makes suicide virtually justifi able in any case. [8]

The role of palliative care

It is often argued that pain and suffering experienced by patients can be relieved by administering appropriate palliative care, making euthanasia a futile measure. [3] According to Norval and Gwynther [4] “requests for euthanasia are rarely sustained after good palliative care is established.”

The rights of vulnerable patients

If euthanasia were to become an accepted practice, it may give rise to situations that undermine the rights of vulnerable patients. [11] These include coercion of patients receiving costly treatments to accept euthanasia or physician-assisted suicide.

The doctor-patient relationship and the physician’s role

Active voluntary euthanasia and physician-assisted suicide undermine the doctor-patient relationship, destroying the trust and confi dence built in such a relationship. A doctor’s role is to help and save lives, not end them. Casting doctors in the role of administering euthanasia “would undermine and compromise the objectives of the medical profession.” [1]

Conclusion

It can be seen that euthanasia is indeed a contentious issue, with the heart of the debate lying at active voluntary euthanasia and physicianassisted suicide. Its legal status in Australia is that of a criminal off ence, conferring murder or manslaughter charges according to the criminal legislation and/or common law across Australian states. Australia’s prohibition and criminalisation of the practice of euthanasia and assisted suicide refl ects the legal status quo that is present in most other countries around the world. In contrast, there are only a few countries and states that have legalised acts of euthanasia and/or assisted suicide. The many arguments that have been put forward for and against euthanasia, and the handful that have been outlined provide only a glimpse into the ethical debate and controversy surrounding the topic of euthanasia.

Conflicts of interest

None declared.

Correspondence

N Ebrahimi: nargus.e@hotmail.com

References

[1] Bartels L, Otlowski M. A right to die? Euthanasia and the law in Australia. J Law Med. 2010 Feb;17(4):532-55.

[2] Walsh D, Caraceni AT, Fainsinger R, Foley K, Glare P, Goh C, et al. Palliative medicine. 1st ed. Canada: Saunders; 2009. Chapter 22, Euthanasia and physician-assisted suicide; p.110-5.

[3] Goldman L, Schafer AI, editors. Goldman’s Cecil Medicine. 23rd ed. USA: Saunders; 2008. Chapter 2, Bioethics in the practice of medicine; p.4-9.

[4] Norval D, Gwyther E. Ethical decisions in end-of-life care. CME. 2003 May;21(5):267-72.

[5] Kerridge I, Lowe M, Stewart C. Ethics and law for the health professions. 3rd ed. New South Wales: Federation Press; 2009.

[6] Legemaate J. The dutch euthanasia act and related issues. J Law Med. 2004 Feb;11(3):312-23.

[7] Bulow HH, Sprung CL, Reinhart K, Prayag S, Du B, Armaganidis A, et al. The world’s major religions’ points of view on end-of-life decisions in the intensive care unit. Intensive Care Med. 2008 Mar;34(3):423-30.

[8] Somerville MA. “Death talk”: debating euthanasia and physician-assisted suicide in Australia. Med J Aust. 2003 Feb 17;178(4):171-4.

[9] Callahan D. When self-determination runs amok. Hastings Cent Rep. 1992 Mar- Apr;22(2):52-55.

[10] Patterson R, George K. Euthanasia and assisted suicide: A liberal approach versus the traditional moral view. J Law Med. 2005 May;12(4):494-510.

[11] George R J, Finlay IG, Jeff rey D. Legalised euthanasia will violate the rights of vulnerable patients. BMJ. 2005 Sep 24;331(7518):684-5.

[12] Rachels J. Active and passive euthanasia. N Engl J Med. 1975 Jan 9;292(2):78-80.

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Graded exposure to neurophobia: Stopping it affect another generation of students

Neurophobia

Neurophobia has probably afflicted you at some stage during your medical school training, whether figuring out how to correlate signs elicited from examination with a likely diagnosis, or deciphering which tract has decussated at a particular level in the neuroaxis. The disease definition of neurophobia as the ‘fear of neural sciences and clinical neurology’ is a testament to its influence; affecting up to 50% of students and junior doctors at least once in their lifetime. [1] The severity of the condition ranges from simple dislike or avoidance of neurology to sub-par clinical assessment of patients with a neurological complaint. Neurophobia is often compounded by a crippling lack of confi dence in approaching and understanding basic neurological concepts.

According to the World Health Organisation, neurological conditions contribute to about 6.3% of the global health burden and account for as much as twelve percent of global mortality. [2] Given these figures, neurophobia persisting into postgraduate medical years may adversely infl uence the treatment that the significant proportion of patients who present with neurological complaints receive. This article will explore why neurophobia exists and some strategies in remedying it from both a student and teaching perspective.

Perceptions of neurology

One factor contributing to the existence of neurophobia is the perception of neurology within the medical community. The classic stereotype, so vividly depicted by the editor of the British Medical Journal: ‘the neurologist is one of the great archetypes: a brilliant, forgetful man with a bulging cranium….who….talks with ease about bits of the brain you’d forgotten existed, adores diagnosis and rare syndromes, and – most importantly – never bothers about treatment.’ [3] The description by Talley and O’ Connor is that of the neurologist being identified by the presence of hatpins in their expensive suits; and how they use the keys of an expensive motor car to elicit plantar reflexes further solidifies the mythology of the neurologist as a stereotype for another generation of Australian medical students. [4] Some have even proposed that neurologists thrive in a specialty known for its intellectual pursuits and exclusivity – a specialty where ‘only young Einsteins need apply.’ [5] Unfortunately, these stereotypes may only serve to perpetuate the reputation of neurology as a difficult specialty, which is complex and full of rare diagnoses (Figure 1).

However, everyone knows that stereotypes are almost always inaccurate. An important question is what do students really think about neurology? There have been several questionnaires asking this question to medical students across various countries and the results are strikingly similar in theme. Neurology is considered by students as the most difficult of the internal medicine specialities. Not surprisingly, it was also the specialty perceived by medical students as the one they had the least knowledge about and, understandably, were least confident in. [5-10] Yet such sentiments are also shared amongst residents, junior doctors and general practitioners in the United Kingdom (UK) and United States (US). [8-10] The persistence of this phenomenon after medical school is supported by the number of intriguing and difficult case reports published in the prestigious Lancet journal. Neurological cases (26%) appear at more than double the frequency of the next highest specialty, gastroenterology, (12%) as a proportion of total case reports in the Lancet from 2003 to 2008. [11] However, this finding may also be explained by the fact that in one survey, neurology was ranked as the most interesting of specialities by medical students, especially after they had completed a rotation within the specialty. [10] So whilst neurophobia exists, it is not outlandish to claim that many medical students do at least find neurology very interesting and would therefore actively seek to improve their understanding and knowledge.

The perception of neurological disease amongst students and the wider community can also be biased. Films such as The Diving Bell and the Butterfly (2007), which is about locked-in syndrome, are not only a compelling account of a peculiar neurological disease, capturing the imagination of the public, but they also highlights the absence of effective treatment following established cerebral infarction. Definitive cures for progressive illnesses, including multiple sclerosis and motor neuron disease are also yet to be discovered, but the reality is that there are numerous effective treatments for a variety of neurological complaints and diseases. Some students will thus incorrectly perceive that the joy gained from neurology only comes from the challenge of arriving at a diagnosis rather than from providing useful treatment to patients.

 

Other causes of neurophobia

Apart from the perception of neurology, a number of other reasons for students’ neurophobia and the perceived difficulty of neurology have been identified. [5-10] Contributory factors to neurophobia can be divided into pre-clinical and clinical exposure factors. Preclinical factors include inadequate teaching in the pre-clinical years, insufficient knowledge of basic neuroanatomy and neuroscience, as well as difficulty in correlating the biomedical sciences with neurological cases (especially localising lesions). Clinical exposure factors include the length of the neurology examination, a perception of complex diagnoses stemming from inpatients being a biased sample of neurology patients, limited exposure to neurology and a paucity of bedside teaching.

Preventing neurophobia – student and teacher perspective

It is clearly much better to prevent neurophobia from occurring than to attempt to remedy it once it has become ingrained. Addressing pre-clinical exposure factors can prevent its development early during medical school. Media reports have quoted doctors and students bemoaning the lack of anatomy teaching contact hours in Australian medical courses. [12, 13] Common sense dictates that the earlier and more frequent the exposure that students have with basic neurology in their medical programs (for example, in the form of introductory sessions on the brain, spinal cord and cranial nerves that are reinforced later down the track), the greater the chance of preventing neurophobia in their clinical years. It goes without saying that a fundamental understanding of neuroanatomy is essential to localising lesions in neurology. Clinically-relevant neurosciences should likewise receive emphasis in pre-clinical teaching.

Many neurology educators concur with students’ wishes for the teaching of basic science and clinical neurology to be effectively integrated . [14, 15] This needs to be a priority. The problem or case based learning model adopted by many undergraduate programs should easily accommodate this integration, using carefully selected cases that can be reinforced with continual assessments via written or observed clinical exams. [15] Neuroanatomy can be a complex science to comprehend. Therefore, more clinically-appropriate and student offerocused rules or tricks should be taught to simplify the concepts. The ‘rule of fours’ for brainstem vascular syndromes is one delightful example of such a rule. [16] This example of a teaching ‘rule’ would be more useful for students than memorising anatomical mnemonics, which favour rote learning over developing a deeper understanding of anatomical concepts. Given the reliance on more and more sophisticated neuroimaging in clinical neurology, correlating clinical neuroimaging with the relevant anatomical concepts must also be included in the pre-clinical years.

During the clinical years, medical students ideally want more frequent and improved bedside teaching in smaller tutorial groups. The feasibility of smaller groups is beyond the scope of my article but I will emphasise one style of bedside teaching that is most conducive to learning neurology. Bedside teaching allows the student to carry out important components of a clinical task under supervision, test their understanding during a clinical discussion and then reflect on possible areas of improvement during a debrief afterwards. This century-old style of bedside teaching, which has more recently been characterised in educational theory as the application of an experiential learning cycle (ELC) framework, works for students and as it did for their teachers when they themselves were students of neurology. [17, 18] The essential questions for a clinical teacher to ask during bedside tutorials are ‘why?’ and ‘so what?’ These inquiries will gauge students’ deeper understanding of the interactions between an illness and its neuro-anatomical correlations, rather than simply testing recall of isolated medical facts. [19]

There is also the issue of the inpatient population within the neurology ward. The overwhelming majority of patients are people who have experienced a stroke and, in large tertiary teaching hospitals, there will also be several patients with rare diagnoses and syndromes. This selection of patients is unrepresentative of the broad nature of neurological presentations and especially excludes patients whose conditions are non-acute and who are referred to outpatients’ clinics. Students are sometimes deterred by patients with rare syndromes that would not even be worth mentioning during a differential diagnosis list in an objective structured clinical examination. Therefore, more exposure to outpatient clinics would assist students to develop skills in recognising common neurological presentations. The learning and teaching of neurology at outpatients should, like bedside tutorials, follow the ELC model. [18] Outpatient clinics should be made mandatory within neurology rotations and rather than making students passive observers, as is commonplace, students should be required to see the patient beforehand (especially if the patient is a patient known to the neurologist with signs or important learning points that can be garnered in their history). A separate clinic room for the student is necessary for this approach, with the neurologist then coming in after a period of time, allowing the student to present their findings followed by an interactive discussion of relevant concepts. Next, the consultant can conduct the consultation with the student observing. Following feedback, the student can think about what can be improved and plan the next consultation, as described in the ELC model (Figure 2). Time constraints make teaching difficult in outpatient settings. However, with this approach, when the student is seeing the known patient by themselves, the consultant can see other (less interesting) patients in the clinic so in essence no time (apart from the teaching time) is lost. This inevitably means the student may miss seeing every second patient that comes to the clinic but in this case, sacrificing quantity for quality of learning may be more beneficial in combating neurophobia long term.

Neurology associations have developed curricula in the US and UK as a “must-know” guideline for students and residents. [20, 21] The major benefits of these endeavours are to set a minimum standard across medical schools and provide clear objectives to which students can aspire. This helps develop recognition of common neurological presentations and the acquisition of essential clinical skills. It is for this reason that the development of a uniform neurology curriculum adopted through all medical school programs across Australia may also alleviate neurophobia.

The responsibility to engage or seek learning opportunities in neurology, to combat neurophobia, nevertheless lies with the students. Students’ own motivation is vital in seeking improvement. It is often hardest to motivate students who find neurology boring and thus fail to engage with the subject. Nevertheless, interest often picks up once students feel more competent in the area. To help improve knowledge and skills in neurology, students can now use a variety of resources apart from textbooks and journals to complement their clinical neurology exposure. One growing trend in the US is the use of online learning and resources for neurology. A variety of online resources supplementing bedside learning and didactic teaching (e.g. lectures) is beneficial to students because of the active learning process they promote. This involves integrating the acquisition of information, placing it in context and then using it practically in patient encounters. [9] Therefore, medical schools should experiment with novel resources and teaching techniques that students will find useful – ‘virtual neurological patients’, video tutorials and neuroanatomy teaching computer programmes are all potential modern teaching tools. This new format of electronic teaching is one way to engage students who otherwise are uninterested in neurology. In conclusion, recognising the early signs of neurophobia is important for medical students and teachers alike. Once it is diagnosed, it is the responsibility of both student and   teacher to minimise the burden of disease.

Acknowledgements

The author would like to thank May Wong for editing and providing helpful suggestions for an earlier draftof the article.

Conflicts of interest

None declared.

Correspondence

B Nham: benjaminsb.nham@gmail.com

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Immunology beyond a textbook: Psychoneuroimmunology and its clinical relevance for psychological stress and depression

Our medical studies encompass many areas of medical science, and immunology is an example of just one. Traditionally, we have been taught that our immune system exists to protect us from pathogens; however, in recent years, this romantic view of the immune system has been challenged and it is now well recognised that it is also involved in whole-body homeostasis and cross talks to other regulating systems of the body. This is the notion of psychoneuroimmunology (PNI). This text will briefly review the current understanding of PNI and how it features prominently in clinical practice as a part of the ‘whole person’ model of patient care and, especially, in terms of stress and depression. With this in mind, PNI is an emerging medical discipline that warrants integration and consideration in future medical care and practice.

Introduction

At first glance, immunology may be viewed by some as an esoteric medical science that simply provides us with the molecular and cellular mechanisms of disease and immunity. It is a subject that all medical students have to face and no doubt can find quite challenging as well. Yet, in recent times, its role in helping us understand mental health and why individuals behave in certain ways has become increasingly appreciated. [1,2] The novel area of study that attempts to explain this intricate and convoluted relationship between the mind, behaviour, nervous system, endocrine system and finally the immune system is, quite appropriately, termed psychoneuroimmunology (PNI) or sometimes psychoendoneuroimmunology. [3] This was probably something that was never mentioned during our studies because it is quite radical and somewhat ambiguous. So what, then, is PNI all about and why is it important?

Many of us may have come across patients that epitomise the association between mental disturbances and physical manifestations of disease. Indeed, it is this biopsychosocial model that is well documented and instilled into the minds of medical students. [4-7] The mechanism behind this, although something best left to science, is nonetheless interesting to know and appreciate as medical students. This is PNI.

The basic science of psychoneuroimmunology

History

The notion that behaviour and the manifestation of disease were linked was probably first raised by Galen (129-199 AD) who noticed that melancholic women were more likely to develop breast cancer than sanguine women. [8] The modern push for PNI probably began in the 1920s to 1930s when Metal’nikof and colleagues conducted several preliminary experiments in various animals showing that the immune system can be classically conditioned. [9] New interest in this area was established by Solomon et al. who, in 1964, coined the term ‘psychoimmunology’ [10]; however, the concept of PNI was firmly established by the American behavioural scientist Dr Robert Ader in his revolutionary 1981 book, ‘Psychoneuroimmunology.’ This book described the dynamic molecular and clinical manifestations of PNI through various early experiments. [11,12] In one initial experiment, Ader and fellow researchers successfully demonstrated that the immune system can be conditioned, similarly to Metal’nikov. After pairing saccharin with the immunosuppressive agent, cyclophosphamide, and administering this to some rats, they found that saccharin administration alone, at a later date, was able to induce an immunosuppressive state marked by reduced titres of haemagglutinating antibodies to injected sheep erythrocytes. [13]

The authors postulated that non-specific stress associated with the conditioning process would have elicited such a result. By extension and based on earlier research, [14] the authors believed psychological, emotional or physical stress probably act through hypothalamic pathways to induce immunomodulation which manifests itself in various ways. [13]

Stress, depression and PNI

A prominent aspect of PNI focuses on the bi-directional relationship between the immune system and stress and depression, where one affects the other. [4,15] The precise mechanisms are complicated but are ultimately characterised by the stress-induced dysregulation, (either activation or depression), of the hypothalamic-pituitaryadrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes. [16] Because of the pleiotropic effects of these hormones, they can induce a dysfunctioning immune system partly through modulating the concentration of certain cytokines in the blood. [15] Endocrine and autonomic pathways upregulate pro-inflammatory cytokines (such as interleukin (IL)-1β, IL-6 and tumour necrosis factor-α (TNF-α)) that can exert their effects at the brain through direct (i.e., circumventricular organs) and indirect access ports (via aff erent nerve fi bres). [17,18] Such pro-inflammatory cytokines therefore stimulate the HPA axis and activate it leading to the rapid production of corticotropin-releasing hormone. [19-21] Eventually, cortisol is produced which, in turn, suppresses the pro-inflammatory cytokines. Interestingly, receptors for these cytokines have also been found on the pituitary and adrenal glands, thereby serving the ability to integrate neuroendocrine signals at all three levels of the HPA axis. [21,22] Cortisol also has significant eff ects on mood, behaviour and cognition. On a short-term basis, it may be beneficial; making an animal more alert and responsive. However, increased periods of elevation may give rise to impaired cognition, fatigue and apathy. [23]

In the brain, an active role is played by the once-thought insignificant glial cells which participate at the so-called tripartite synapse (glial cell plus pre- and post-synaptic neurons). [24] It is this unit that is fundamental to much of the central nervous system activity of the PNI system. Pro-inflammatory cytokines like interferon (IFN)-α and IL-1β released from peripheral and central (microglia and astrocytes) sources can alter dopaminergic signals, basal ganglial circuitry, hippocampal functioning and so on. Consequently, this induces behavioural changes of anhedonia, memory impairment and other similar behaviours. [18,25] Since IFN-α receptors have been found on microglia in the brain, [26] IFN-α likely also causes further local inflammation and further disruption of dopaminergic signals. Excessively activated microglia by a range of inflammatory cytokines can therefore cause direct neurotoxicity and neuropathology. [27] Additionally, these cytokines can induce activity of the indoleamine 2,3-dioxygenase enzyme (found in astrocytes and microglia) which metabolise the precursor of serotonin, tryptophan. The result is a reduction of serotonin and the production of various products, including quinolinic acid, an NMDA (N-methyl-D-aspartate) receptor agonist which leads to excess glutamate and neurodegeneration. These mechanisms are postulated to contribute to the pathogenesis of depression; however, the precise mechanisms of which are yet to be fully elucidated. [28-30]

Recent research into behavioural epigenetics has also provided an additional interesting link whereby stressors to the psychosocial environment can modulate gene expression within the neuroimmune, physiological and behavioural internal environments. This may account for the long-term aforementioned changes in immune function. [31]

Depression has also been shown to activate the HPA and SAM axes as well through inflammatory processes, [28,32] which in turn exacerbates any pre-existing depressive behaviours. [33] This inflammatory theory of depression sheds light onto the complicated pathophysiology of depression, adding to the already well-characterised theory of serotonergic neurotransmission deficiency. [28,33] Interestingly, proinfl ammatory cytokines have been shown to modulate serotonergic activity in the brain as well, [34,35] which provides further insight into this complex disorder. There is question as to whether or not this may have its roots with evolution where the body diverts energy resources away from other areas to the immune system for the promotion of anti-pathogenic activity during stress and depression. [17] For instance, with threat of an injury or wound in an acute situation (the stressor), cortisol (a natural immunosuppressant) would be released via the HPA axis. This aids in energy conservation which in turn, and paradoxically, attempts to minimise the non-helpful effect of immunosuppression in times of infection risks. [17] Depressive behaviour such as lethargy has also been said to have stemmed from the need to conserve energy to promote fever and inflammation. [2] Ultimately, the evolutionary aspects of PNI are under current speculation and investigation to elicit the precise links and relationships. [36]

The alterations of the immune system in stress and depression have implications for other areas of medicine as well. Though conclusive clinical experiments are lacking, it has been strongly hypothesised that this imbalanced immune state can contribute to a plethora of medical ailments. Depression, characterised by a general pro-inflammatory state with oxidative and nitrosative stress, [33,37] can contribute to poor wound healing; and exacerbate chronic infections and pain. [38,39] Stress similarly entails a dysregulated immune system and may contribute to the aforementioned conditions plus cardiovascular disease and minor infectious diseases such as the common cold. [40- 44] The link with cancer is somewhat more controversial but both may, in some way, predispose to the development of it through numerous mechanisms such as reduced immune surveillance by immune cells (cytotoxic T cells and natural killer cells), general inflammation and genomic instability. [45,46]

Highlighting the bidirectionality of the PNI paradigm, secondary inflammation caused by a myriad of neurological diseases (e.g., Huntington’s disease, Alzheimer’s disease) and local and systemic disorders (e.g., systemic lupus erythematosus, stroke, cardiovascular disease and diabetes mellitus) may very well contribute to the pathogenesis of co-existing depression. [47] This may account for the close association of depression and such diseases. Underlying neurochemical changes have been observed in many of these diseases—especially the neurological disease examples—and it has been suggested that depression vulnerability is proportional to how well one can ‘adapt’ to said neurochemical imbalances. [48,49]

Through an immunophysiological point-of-view, these links certainly makes sense; but it is important to note that there could be other confounding factors, such as increased alcohol consumption and other associated behaviours that accompany stress and depression that can contribute to pathology. [50] The question therefore remains as to how much the mind plays in the pathogenesis of physical ailments. Figure 1 summarises the general PNI model as it relates to stress and depression.

Implications

Having explored the discipline of PNI, what is the importance of this for clinical practice? Because of the links between stress and depression; altered immunity; other ill-effects and behaviour, [3,12] it seems fitting that if we can address a patient’s underlying stress or depression, we may be able to improve the course of their illness or prevent, to a certain extent, the onset of certain diseases by correcting immune system dysregulation. [43]

Simply acknowledging the relationship between stress and their role in the pathogenesis, maintenance and susceptibility of diseases is certainly not enough, and healthcare professionals should consider the mental state of mind for every patient that presents before them. It is fortunate, then, that a myriad of simple stress-management strategies could be employed to improve their mental welfare, depending on their individual circumstances. Such strategies include various relaxation techniques, meditation, tai chi, hypnosis and mindfulness practice. These have, importantly, proven cost-eff ective and lead to self-care and self-efficacy. [51,52]

As an example, mindfulness has received considerable attention in its role of alleviating stress and depression. [52] Defined as the increased awareness and attention to present, moment-to-moment thoughts and experiences, mindfulness therapy has shown remarkable efficacy in the promotion of positive mental states and quality of life. [52-54] This is particularly important in this age of chronic diseases and their associated unwelcomed psychological consequences. [54] Furthermore, and in light of the discussion above on PNI, there is evidence that mindfulness practice induces physiological responses in brain and immune function. [55,56] This suggests that its benefits are mediated, at least in part, through such positive immunological alterations that modulate disease processes.

With the growing understanding of the cellular and molecular mechanisms behind stress, depression and other similar psychiatric disorders, a host of novel pharmacological interventions to target the previously discussed biological pathways are actively being researched. Most notably is the proposition of the role of anti-inflammatories in ameliorating such conditions where patients present in an increased inflammatory state. This is largely based on experimental work where antagonists to pro-inflammatory cytokines and/or their receptors improve sickness behaviours in animals. [17] As an example, the cholesterol-lowering statins have been found to have intrinsic anti- inflammatory and antioxidant properties. In a study of patients taking statins for cardiovascular disease, it was found that statins had a substantial protective effect on the risk of developing depression. This suggests that the drug acts, at least in part, to decrease systemic inflammatory and oxidative processes that characterise depression. [57] Other drugs being researched aim to tackle additional pathways such as those involving neurotransmitters and their receptors.

Of the neuroendocrine arm of PNI, current research is looking at ways to reverse HPA axis activation. [20] Some tested drugs that act on specific parts of the HPA axis seem to show promise; however, a major problem is tailoring the correct drug to the correct patient, for not all patients will present with the same neuroendocrine profile. [58,59] Neuroendocrine manipulation can also be used to treat or act as an adjunct to other non-HPA axis-mediated diseases. For example, administration of melatonin and IL-2 was able to increase the survival time in patients with certain solid tumours. [60] Needless to say, a great amount of research is further warranted to test and understand possible pharmaceutical agents.

Discussion and Conclusion

The exciting and revolutionary field of PNI has now provided us with the internal links of all the major regulating systems of the human body. The complex interactions that take place is, indeed, a tribute to the complexity of our design, and has provided a basis or mechanism of how our mind and behaviour can infl uence our physical health. As a result, serious stressors—be them emotional, mental or physical—can wreak havoc on our delicate internal environment and predispose to physical ailments, which can further exacerbate the inciting stressors and our mental state. For said psychological stress or depression, it seems appropriate that if healthcare professionals can ameliorate the severity of these, they may be able to further improve the physical health of an individual. How much so is a matter of debate and further investigation. Conversely, as demonstrated by the bi-directionality model of PNI, addressing or ‘fi xing’ the organic pathology may be conducive to the mental state of patients’ minds.

Whilst clinical approaches have been sharply juxtaposed to a very theoretical and scientific review of PNI, this has been deliberately done to hopefully demonstrate how mind-body therapies can exert their physical benefits. Accordingly, valued mind-body therapies deserve as much attention as the scientific study of molecular pharmacology. It is also important to note that even these two approaches (pharmacology and mind-body therapies) are almost certainly the tip of the iceberg; for there is certainly a vast amount more to be further explored in our therapeutic approach to medical conditions. For example, how does a practitioner-patient relationship fit into this grand scheme of things, and how much of a role does it play? No doubt a decent part for sure. Furthermore, whilst the PNI framework provides good foundations for which to explain, (at a basic level), the mechanisms behind the development of stress, depression and associated ailments, further insight is needed into the biological basis of these. For example, a symphony of intricate factors (such as the up-regulation of inflammation-induced enzymes, neurotransmitter changes, dysfunction of intracellular signalling, induced autoimmune activity, neurodegeneration and decreased serum levels of antioxidants and zinc) are at play for the signs and symptoms of depression. [61,62] Thus, the complex pathogenesis of psychological stress and depression begs for further clinical and scientific research into unravelling its mysteries. Nevertheless, with a sound basis behind mindfulness, other similar mind-body therapies and novel pharmacological approaches, it seems suitable for these to be further integrated into primary care [54] and other areas of medicine as an adjuvant to current treatments. If we can achieve this, then medicine undoubtedly has more potent tools in its armamentarium of strategies to address and alleviate the growing burden of chronic disease.

Acknowledgements

My thanks go to Dr E Warnecke and Prof S Pridmore for their support.

Conflicts of interest

None declared.

Correspondence

A Lee: adrian.lee@utas.edu.au

Categories
Articles Feature Articles

Is there a role for end-of-life care pathways for patients in the home setting who are supported with community palliative care services?

The concept of a “good death” has developed immensely over the past few decades and we now recognise the important role of palliative care services in healthcare for the dying, our most vulnerable population. [1-3] In palliative care, end-of-life care pathways have been developed to transfer the gold standard hospice model of care for the dying to other settings, addressing the physical, psychosocial and practical issues surrounding death. [1,4] Currently, these frameworks are used in hospitals and residential aged-care facilities across Australia. [1] However, there is great potential for these pathways to be introduced into the home setting with support from community palliative care services. This could help facilitate a good death for these patients in the comfort of their own home, and also support their families through the grieving process.

Although there is no one definition of a “good death”, many studies have examined factors considered important at the end-of-life by patients and their families. Current literature acknowledges that terminally ill patients highly value adequate pain and symptom management, avoidance of prolongation of death, preparation for end-of-life, relieving the burden imposed on their loved ones, spirituality, and strengthening relationships with health professionals through acknowledgement of imminent death. [2] Interestingly, the Steinhauser study noted a substantial disparity in views on spirituality between physicians and patients. [3] Physicians were found to rank good symptom control as most important, whilst patients considered spiritual issues to hold equal significance. These studies highlight the individual nature of end-of-life care, which refl ects why the holistic approach of palliative care can improve the quality of care provided.

It is recognised that patients with life-limiting illnesses have complex needs that often require a multidisciplinary approach with multiple care providers. [1] However, an increased number of team members also creates its own challenges, and despite the best intentions, care can often become fragmented due to poor interdisciplinary communication. [5] This can lead to substandard end-of-life care with patients suff ering prolonged and painful deaths, and receiving unwanted, expensive and invasive care, as demonstrated by the Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT). [6] Temel et al. also demonstrated that palliative care can improve the documentation of advanced care directives. [7] For terminally ill patients, this is essential in clarifying and enabling patients’ wishes regarding end-of-life to be respected.

In 2010, Temel et al. conducted a randomised controlled trial in patients with newly diagnosed metastatic non-small-cell lung cancer, comparing the effect of palliative care and standard oncologic therapy, to standard oncologic therapy alone. [7] Results demonstrated that palliative care intervention improves quality of life and reduces rates of depression, consistent with existing literature. [7] Furthermore, despite receiving less aggressive end-of-life care, the additional early involvement of palliative care services resulted in a significant prolongation of life, averaging 2.7 months (p = 0.02). [7] This 30% improved survival benefit is equivalent to that achieved with a response to standard chemotherapy regimens, which has profound significance for patients with metastatic disease. [7] This study thereby validates the benefits of early palliative care intervention in oncology patients. In addition, early palliative intervention encourages advance care planning, allowing treating teams to elicit and acknowledge patient preferences regarding end-of-life care.

Many physicians often find it difficult to discuss poor prognoses with patients, potentially leaving patients and their families unaware of their terminal condition, despite death being anticipated by the treating team. [1,4] Many health care professionals are uncomfortable discussing death and dying, citing lack of training and fear of upsetting the patient. [8] Regardless, patients are entitled to be informed and supported through this difficult time. In addition, terminal patients and their caregivers are often neglected in decisions about their care, [9] despite their fundamental legal and ethical right to be involved, and studies indicate that they often want to be included in such discussions. [1,10,11] With the multitude of patient values and preferences for care, it can often be difficult to standardise the care provided. End-of-life care pathways encourage discussion of prognosis, facilitating communication that allows patients’ needs to be identified and addressed systematically and collaboratively. [1]

End-of-life care pathways provide a systematic approach and a standardised level of care for patients in the terminal phase of their illness. [1] This framework includes documentation of discussion with the patient and carers of the multi-disciplinary consensus that death is now imminent and life-prolonging treatment is futile, and also provides management strategies to address the individual needs of the dying. There is limited evidence to support the use of end-of-life care pathways, however we cannot discount the substantial anecdotal benefits. [1,12] The lack of high-quality studies indicates a need for further research. [1,12] When used in conjunction with clinical judgment, these pathways can lead to benefits such as: improved symptom control, earlier acknowledgement of terminal prognosis by the patient and family, prescription of medications for end-of-life, and aiding the grieving process for relatives. [1,12,13] As such, end-of-life care pathways are highly regarded in palliative care, transferring the benchmarked hospice model of care of the dying into other settings, [14] and have been widely implemented nationally and internationally. [1]

The most recognised and commonly used end-of-life care pathway is the Liverpool Care Pathway (LCP), which was developed in the United Kingdom to transfer the hospice model of care for the dying to other care settings. [13,15] It has been implemented into hospices, hospitals and aged care facilities, and addresses the physical, psychosocial and spiritual needs of these patients. [1,13,15] In 2008, Verbeek et al. examined the effect of the LCP pre- and post-implementation on patients from hospital, aged care and home settings. [13] Results demonstrated improved documentation and reduced symptom burden as assessed by nurses and relatives, in comparison with the baseline period. [13] Although increased documentation does not necessarily equate to better care, high-quality medical records are essential to facilitate communication between team members and ensure quality care is provided. In this study, staff also reported that they felt the LCP provided a structure to patient care, assisted the anticipation of problems, and promoted proactive management of patient comfort. [13] The LCP has significantly increased the awareness of good terminal care, and has provided a model for the end-of-life care pathways currently in use in hospitals and institutions throughout Australia. [1,4]

Community palliative care services support terminally ill patients at home in order to retain a high quality of life. Recognising the holistic principles of palliative care, these multidisciplinary teams provide medical and nursing care, counselling, spiritual support and welfare supports. In the Brumley trial, which evaluated an in-home palliative care intervention with a multidisciplinary team for homebound terminally ill patients, results demonstrated that the intervention group had greater satisfaction with care, were less likely to visit the emergency department, and were more likely to die in the comforts of their own home. [16] These results infer that the community palliative care team provided a high standard of care where symptoms were well-managed and did not require more aggressive intervention. This prevented unnecessary emergency presentations, potential distress for the patient and family, and allowed better use of resources. This study demonstrates that community palliative care services can significantly improve the quality of care for patients living at home with life-limiting illnesses, however, there is still scope for improvement in the current healthcare system.

End-of-life care pathways are regarded as best practice in guiding care for patients where death is imminent. [1] In Australia, there are a number of these frameworks that have been implemented in hospitals and aged-care facilities, demonstrating an improvement in the quality of care in these settings. However, there are also many terminally ill patients who choose to reside in the comfort of their own home, and are supported by community palliative care services. End-of-life care pathways support a high standard of care, which should be available to all patients, irrespective of where they choose to die. As such, there may be a role for end-of-life care pathways in the home setting, supported by community palliative care services. Introducing already implemented local end-of-life care pathway into the community has great potential to reap similar benefits. Initially, these frameworks would be implemented by the community palliative care team, however, caregivers could be educated and empowered to participate in the ongoing care. This could be a useful means to facilitate communication between treating team members and family, and also empower the patient and family to become more involved in their care.

The potential benefits of implementing end-of-life care pathways into community palliative care services include those currently demonstrated in the hospital and aged-care settings, however there are potentially further positive effects. By introducing these frameworks into the homes of terminally ill patients, caregivers can also be encouraged to take a more active role in the care of their loved ones. This indirect education for the patient and family can provide a sense of empowerment, and assist them to make informed decisions. Additional potential benefits of these pathways could include a reduction in the number of hospital admissions and emergency department presentations, which would reduce the pressures on our already overburdened acute care services. Empowered family and carers could also assist with monitoring, providing regular updates to the community palliative care team, which could potentially lead to earlier detection for when more specialised care is required. The documentation within the pathways could also allow for a smoother transition to hospices if required, and prevent unnecessary prolongation of death. This may translate to prevention of significant emotional distress for the patient and family in an already difficult time, and promote more effective use of limited hospital resources. Integrating end-of-life care pathways into community palliative care services has many potential benefits for patients at home with terminal illnesses, and should be considered as an option to improve the delivery of care.

Palliative care can significantly improve the quality of care provided to patients in the terminal phase, which can be guided by end-of-life care pathways. Evidence validates that these pathways encourage a multidisciplinary change in practice that facilitates a “good death”, and supports the family through the bereavement period. In the community, this framework has the potential to empower patients and their caregivers, and assist them to make informed decisions regarding their end-of-life care, thereby preventing unwanted aggressive intervention and unnecessary prolongation of death. However, there is a need for further high-quality studies to validate the anecdotal benefits of these pathways, with potential for a randomised controlled trial investigating the use of end-of-life care pathways in the home setting in Australia. In conclusion, the introduction of end-of-life care pathways into community palliative care services has great potential, particularly if supported and used in conjunction with specialist palliative care teams.

Acknowledgements

I would like to acknowledge Dr Leeroy William from McCulloch House, Monash Medical Centre for his support in developing this proposal, and Andrew Yap for his editorial assistance.

Conflicts of interest

None declared.

Correspondence

A Vo: amanda.vo@southernhealth.org.au

Categories
Book Reviews Articles

The only medical science textbook you need to buy?

Wilkins R, Cross S, Megson I, Meredith D. Oxford Handbook of Medical Sciences, Second Edition. Oxford: Oxford University Press; 2011.

RRP: $47.95

A complete guide to the medical sciences that fits in your pocket? Including anatomy? It sounds like something you’d find on the bookshop shelf between Refl exology at Your Fingertips and Sex Explained. But The Oxford Handbook of Medical Sciences (OHMS) is probably one of the few serious books that handles this enormous topic and can still be picked up with one hand. The first edition was published in 2006, and it’s been a fairly constant companion since I started graduate medicine at Sydney University. The dense but well written text often feels more conducive to medical school than authoritative textbooks – if you’re asked to explain a concept in a tutorial, the 30 second answer is better than the five minute dissertation. Compiling principles and systems also means you can flip from say anatomy to immunology without piling up your desk with resources. Unfortunately, the more I’ve used the first edition the more niggling errors I’ve come across. Granted most are just typos, but others were more frustrating. Including a colour DNA sequencing output that seems more CSI-prop than medical text, at least to someone with a molecular biology background. And errors like labelling the muscles of mastication as supplied by cranial nerve VIII are inexcusable (instead of V3 mandibular – so presumably type-setting error). So OHMS1e – a great book in serious need of a revision, but could the second edition be the last medical science book you ever buy?

The OHMS second edition was published September 2011 from $35 in online bookshops. On first impression it has not transformed into a full colour extravaganza like the latest Oxford Handbooks of Clinical Medicine/Specialties. It is 40 pages longer than the original, 962 in total, and still small enough for a big pocket. Much of the first edition worked well and it is good to see that the layout remains the same, with each topic generally covered in two pages or less, with plenty of room for annotation. The first three chapters cover the essentials: cells, molecules and biochemistry – with some good looking new figures. The ten systems-based chapters are now followed by a chapter on medicine and society. The final chapter – techniques of medical sciences – has had a timely rewrite, it won’t make you a lab scientist but at least you’ll be able to have an intelligent conversation with someone who is. The best addition, in my opinion, are the blue boxes succinctly summarising relevant treatments and drug therapies in all the sections.

The cross-referencing to the most recent clinical Oxford Handbooks is a welcome update (in spite of a couple that refer to OHCM8p.000). I would have liked to see a more thorough reworking of the anatomy section; the diagram of the muscles of the hand remains duplicated a few pages apart. The molecular biology chapter, the one I feel semi-qualified to comment on, is my major complaint. There is no mention of new sequencing technologies and of non-coding RNAs that we are frequently told are the future of the field. Instead Maxam-Gilbert sequencing, a technique probably last done in the 1980s is still covered. Furthermore, ‘junk DNA’, a term surely killed off by the ENCODE project, makes a vampirelike appearance here. [1]

In summary, if you’ve already built a reasonable understanding of the medical sciences and are looking for a one-stop book for reference or revision on the run then this book is a good option. For its convenience and conciseness it is hard to beat OHMS2e. The USMLE crammers like First Aid, offer analogous coverage at an equivalent price but carrying one in your pocket isn’t an option. But beware – as far as OHCM2e is concerned the muscles of mastication are still innervated by CNVIII. Now where is my anatomy book?

References

[1] Myers RM, Stamatoyannopoulos J, Snyder M, Dunham I, Hardison RC, Bernstein BE, et al. A user’s guide to the encyclopedia of DNA elements (ENCODE). PLoS Biol 2011 Apr;9(4):e1001046.

Categories
Book Reviews Articles

Harrison’s: Friend or Foe?

Longo DL, Harrison TR. Harrison’s Principles of Internal Medicine, Eighteenth Edition. London: McGraw-Hill; 2012.

RRP: $199

So a review of this text has been done before, not of Harrison’s Principles of Internal Medicine (Harrison’s) in isolation but a comparison to William Osler’s The Principles and Practice of Medicine. [1] The latest edition of Harrison’s has been available since July 2011, and as an avid user of the online version of Harrison’s (via AccessMedicine™ through the University’s library website). The book is found in two tomes, a whopping 4012 pages in total. I have a thing for being able to physically hold a book and read it, hence not relying on the online edition, which has been previously compared to the text version, as my internet connection is very erratic and the University has a concurrent users policy. [2]

Alas it was a decision that I do regret (to some extent) as I have since found myself referring to Harrison’s to find an answer to a problem, whether it be electronically via the DVD given with the book or via fl icking through the book itself, and neglecting some other general medicine or specialised texts that I own. This speaks volumes about Harrison’s comprehensive nature, but also about my enjoyment of the text.

So what do I like about the book? It is detailed, this may speak more about myself than the text but I think that many medical students appreciate this level of detail, if only for interest rather than what is actually required. I mean, do you know of any other books with 395 chapters and another 51 chapters available electronically? I love the detailed explanations of concepts such as “Insulin biosynthesis, secretion and action”, which would normally be found in a more specialised text such as Lehninger’s Principles of Biochemistry™, and pathophysiology of common diseases such as asthma, COPD and myocardial infarction. [3]

The “yellow sections” in the chapters are a great reference for medical students and physicians alike, these are the sections on treatment of certain conditions. The diagrams are great, as are flowcharts, which explain key concepts such as development of a certain condition (for example, ischaemic stroke) or treatment or diagnostic algorithms, such as tuberculosis or HIV/AIDS. The layout of the parts, sections and chapters of the text are very logical and (if you were keen enough) could be read in order for example:

“Part 10: Disorders of the cardiovascular system, Section 1: Introduction to cardiovascular disorders, Chapter 224: Basic Biology of the Cardiovascular system, Chapter 225: Epidemiology of Cardiovascular disease … Section 2: Diagnosis of Cardiovascular disorders, Chapter 227: Physical examination of the cardiovascular system, Chapter 228: Electrocardiography … Section 3: Disorders of rhythm … Section 4: Disorders of the heart … Section 5: Vascular disease”

It is easy to see how logically the book is organised, starting from the basics of the given system or group of conditions then working through epidemiology, diagnosis and then fi nally about the conditions themselves; and given that Part 10 of the book as a whole spans pages 1797 – 2082 (yes, 285 pages) you can gather an appreciation for the detail of the text. Another great feature is the “further readings” given at the end of each chapter citing original and review publications from peer reviewed journals so (if interested) you can read some more about the topic you are interested in.

What don’t I like about the book? Having two volumes can sometimes be a little tedious when you pick up one and then find that the topic you want is in the other (although you have to remember page numbers this way, it is still preferable to having one enormous tome with a tiny typeface). The organisation of the text is a double-edged sword as it can get frustrating as when searching for a condition such as polycystic ovarian syndrome (PCOS) this will bring up entries in sections such as: menstrual disorders, biology of obesity, amenorrhoea, metabolic syndrome, hirsutism and virilisation and diabetes mellitus; yet there is no definitive section on PCOS itself as there is for a condition such as phaeochromocytoma. Sometimes you open a page, and the amount of text overwhelms you and there are no figures to break it up, which can be quite intimidating for a medical student to find one specific passage or sentence. This isn’t too large a problem in my opinion, but I have known students to be put off by books of such a nature.

References

[1] Hogan DB. Did Osler suff er from “paranoia antitherapeuticum baltimorensis”? A comparative content analysis of The Principles and Practice of Medicine and Harrison’s Principles of Internal Medicine, 11th edition. CMAJ. 1999 Oct;161(7):842-5.

[2] DeZee KJ, Durning S, Denton GD. effect of electronic versus print format and different reading resources on knowledge acquisition in the third-year medicine clerkship. Teach Learn Med. 2005;17(4):349-54.

[3] Powers AC. “Insulin Biosynthesis, Secretion and Action” from Harrison’s Principles of Internal Medicine. 18 ed. Longo DF, A; Kasper, D; Hauser, S; Jameson, J L; Loscalzo, J, editor. Columbus: McGraw-Hill Medical; 2011.